ArticleOncology reports2017
Inhibition of the HDAC/Suv39/G9a pathway restores the expression of DNA damage-dependent major histocompatibility complex class I-related chain A and B in cancer cells.
Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Dynamic phosphorylation of cGAS by DNA-PKcs and PPP1CC balances DNA repair and innate immunity.Medical oncology (Northwood, London, England) · 2026Article
- Maternal histone methyltransferases antagonistically regulate autosomal random monoallelic expression (aRMAE) in C. elegans.Nature communications · 2025Article
- The Roles of H3K9me3 Writers, Readers, and Erasers in Cancer Immunotherapy.International journal of molecular sciences · 2024Review
- Promising and challenging phytochemicals targeting LC3 mediated autophagy signaling in cancer therapy.Immunity, inflammation and disease · 2024Review
- A chimeric antigen receptor uniquely recognizing MICA/B stress proteins provides an effective approach to target solid tumors.Med (New York, N.Y.) · 2023Article
- Epigenetic modulation and prostate cancer: Paving the way for NK cell anti-tumor immunity.Frontiers in immunology · 2023Review
- Value of carbon-ion radiotherapy for early stage non-small cell lung cancer.Clinical and translational radiation oncology · 2022Review
- The Role of HDACs in the Response of Cancer Cells to Cellular Stress and the Potential for Therapeutic Intervention.International journal of molecular sciences · 2022Review
- Mapping the biogenesis of forward programmed megakaryocytes from induced pluripotent stem cells.Science advances · 2022Article
- Characterizing HDAC Pathway Copy Number Variation in Pan-Cancer.Pathology oncology research : POR · 2022Article
- Radiosensitization effect by HDAC inhibition improves NKG2D-dependent natural killer cytotoxicity in hepatocellular carcinoma.Frontiers in oncology · 2022Article
- G9a: An Emerging Epigenetic Target for Melanoma Therapy.Epigenomes · 2021Article
- Epigenetic regulation of autophagy: A key modification in cancer cells and cancer stem cells.World journal of stem cells · 2021Review
- Rationale of combination of anti-PD-1/PD-L1 antibody therapy and radiotherapy for cancer treatment.International journal of clinical oncology · 2020Review
- High glucose promotes pancreatic cancer cells to escape from immune surveillance via AMPK-Bmi1-GATA2-MICA/B pathway.Journal of experimental & clinical cancer research : CR · 2019Article
- Ex Vivo Expanded Human Vγ9Vδ2 T-Cells Can Suppress Epithelial Ovarian Cancer Cell Growth.International journal of molecular sciences · 2019Article
- Novel Approaches to Improve the Efficacy of Immuno-Radiotherapy.Frontiers in oncology · 2019Review
- Kaempferol induces autophagic cell death via IRE1-JNK-CHOP pathway and inhibition of G9a in gastric cancer cells.Cell death & disease · 2018Article
- NKG2D and its ligands in cancer.Current opinion in immunology · 2018Review
- Unconventional Approaches to Modulating the Immunogenicity of Tumor Cells.Advances in cancer research · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunotherapy is expected to be promising as a next generation cancer therapy. Immunoreceptors are often activated constitutively in cancer cells, however, such levels of ligand expression are not effectively recognized by the native immune system due to tumor microenvironmental adaptation. Studies have demonstrated that natural-killer group 2, member D (NKG2D), a major activating immunoreceptor, responds to DNA damage. The upregulation of major histocompatibility complex class I-related chain A and B (MICA/B) (members of NKG2D ligands) expression after DNA damage is associated with NK cell-mediated killing of cancer cells. However, the regulation of DNA damage-induced MICA/B expression has not been fully elucidated in the context of the types of cancer cell lines. In the present study, we found that MICA/B expression varied between cancer cell lines after DNA damage. Screening in terms of chromatin remodeling identified that inhibitors related to chromatin relaxation via post-translational modification on histone H3K9, i.e. HDAC, Suv39 or G9a inhibition, restored DNA damage-dependent MICA/B expression in insensitive cells. In addition, we revealed that the restored MICA/B expression was dependent on ATR as well as E2F1, a transcription factor. We further revealed that low‑dose treatment of an HDAC inhibitor was sufficient to restore MICA/B expression in insensitive cells. Finally, we demonstrated that HDAC inhibition restored DNA damage‑dependent cytotoxic NK activity against insensitive cells. Thus, the present study revealed that DNA damage‑dependent MICA/B expression in insensitive cancer cells can be restored by chromatin relaxation via the HDAC/Suv39/G9a pathway. Collectively, manipulation of chromatin status by therapeutic cancer drugs may potentiate the antitumor effect by enhancing immune activation following radiotherapy and DNA damage-associated chemotherapy.
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